Abstract：
Novel pathways of vitamin D3, lumisterol 3 (L3), and tachysterol 3 (T3) activation have been discovered, initiated by CYP11A1 and/or CYP27A1 in the case of L3 and T3. The resulting hydroxymetabolites enhance protection of skin against DNA damage and oxidative stress; stimulate keratinocyte differentiation; exert anti-inflammatory, antifibrogenic, and anticancer activities; and inhibit cell proliferation in a structure-dependent manner. They act on nuclear receptors, including vitamin D receptor, aryl hydrocarbon receptor, LXRα/β, RAR-related orphan receptor α/γ, and peroxisome proliferator-activated receptor-γ, with selectivity defined by their core structure and distribution of hydroxyl groups. They can activate NRF2 and p53 and inhibit NF-κB, IL-17, Shh, and Wnt/β-catenin signaling. Thus, they protect skin integrity and physiology.
摘要：
维生素D3，lumisterol3（L3），并且已经发现了速留醇3（T3）的激活，在L3和T3的情况下由CYP11A1和/或CYP27A1启动。产生的羟基代谢物增强皮肤对DNA损伤和氧化应激的保护;刺激角质形成细胞分化;发挥抗炎,抗纤维化，和抗癌活性；并以结构依赖性方式抑制细胞增殖。它们作用于核受体，包括维生素D受体,芳烃受体，LXRα/β，RAR相关孤儿受体α/γ，和过氧化物酶体增殖物激活受体-γ，选择性由它们的核心结构和羟基的分布来定义。它们可以激活NRF2和p53并抑制NF-κB，IL-17嘘,和Wnt/β-连环蛋白信号传导。因此，它们保护皮肤的完整性和生理。
